treatment of right hemispheric cerebral infarction by...

874

Treatment of Right Hemispheric CerebralInfarction by Hemicraniectomy

J.B. Delashaw, MD, W.C. Broaddus, MD, PhD, N.F. Kassell, MD, E.C. Haley, MD,

G.A. Pendleton, RN/CNRN, D.G. Vollmer, MD, W.W. Maggio, MD, and M.S. Grady, MD

An anecdotal series of nine patients (three men and six women with an average age of 57 years)presented with progressive neurologic deterioration while on medical therapy for large righthemispheric cerebral infarction. Clinical signs of uncal herniation (anisocoria or fixed anddilated pupils, and/or left hemiplegia with right decerebrate posturing) were present in sevenof these nine patients. Computerized tomography of the head confirmed mass effect fromcerebral edema. It was the clinical judgment of the treating neurologists and neurosurgeonsthat each of these nine patients would perish unless surgical decompression of the infarctedbrain was performed. Accordingly, each was treated with right hemicraniectomy and dura!augmentation. Six patients demonstrated neurologic improvement on the first postoperativeday. One patient, with a postoperative diagnosis of lung cancer, died 1 month after surgery. Theremaining eight patients are currently living with their families with a follow-up period rangingfrom 5 to 25 months. Patient outcome as evaluated by the Barthel Index indicates that threeindividuals are functioning with minimal assistance and that the remaining six patients arefunctionally dependent After rehabilitative therapy, four patients returned for elective cranio-plasty. These results suggest that hemicraniectomy can be an effective lifesaving procedure formalignant cerebral edema after large hemispheric infarction. (Stroke 1990^1:874-881)

Stroke is the most prevalent disease involvingthe central nervous system. During the acuteperiod following a cerebral infarction, current

medical management is primarily supportive to pre-vent extension of the infarct or the development ofcardiopulmonary complications. Neurologic declineis often attributed to surrounding edema during thisacute infarction period. Fortunately, as the edemaresolves, the patient frequently improves. However,massive unilateral hemispheric cerebral edema candevelop from internal carotid or middle cerebralartery occlusion and can result in uncal herniationand death. Contemporary medical modalities involv-ing steroids, hyperventilation, barbiturates, mannitol,or other antiedema agents are frequently ineffectivein reducing acute cerebral edema following infarc-tion. In those stroke victims with massive unilateralhemispheric edema, surgical decompression by hemi-

From the Department of Neurosurgeiy (J.B.D., W.C.B., N.F.K.,G.A.P., D.G.V., W.W.M., M.S.G.) and the Department of Neu-rology (E.C.H.), University of Virginia Medical Center, Char-lottesville, Virginia.

Presented in abstract form at the 13th International JointConference on Stroke and Cerebral Circulation, San Diego,California, February 18-20, 1988.

Address for correspondence: Neal F. Kassell, MD, Departmentof Neurosurgery, Box 212, University of Virginia Health SciencesCenter, Charlottesville, VA 22908.

Received June 26, 1989; accepted February 28, 1990.

craniectomy may be an effective alternative whenmedical modalities fail. In this study we present ananecdotal series that describes the results of hemi-craniectomy on nine consecutive patients presentingwith progressive neurologic deterioration while onmedical therapy for spontaneous large right hemi-spheric infarctions.

Subjects and MethodsPatients experiencing spontaneous acute cerebral

ischemia and/or infarction were admitted to themedical, neurologic, or neurosurgical services at theUniversity of Virginia, Charlottesville. These patientswere followed by a stroke service comprised of aneurovascular neurologist, a neurosurgeon, andother health care professionals. Stroke was diag-nosed by clinical history, physical examination, andhead computed tomography (CT). Patients diag-nosed with stroke were treated aggressively withadequate hydration and oxygenation. When neces-sary, stroke patients were observed in an intensivecare unit setting, intubated, and ventilated. To avoidanticoagulation therapy, 325 mg aspirin was givendaily to patients demonstrating findings of largecortical infarctions. If a stroke victim began to dem-onstrate neurologic decline, hyperventilation andantiedema agents, such as mannitol and steroids,were implemented. Cerebral hemorrhage and hydro-

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Delashaw et al Hemicraniectomy for Cerebral Infarction 875

TABLE 1. Patient Information

Patient

1

23

4

5

6

7

8

9

Age

(yr)41

48

48

58

58

58

67

68

68

Sex

M

F

M

F

F

M

F

F

F

Admission

5T, Dec11, An14

10T

14

14

14

8T

14

GCS

Before surgery

5T, Dec11, An12, An3T, FD, Dec6T, FD4T, An14, drowsy4T, An6T, FD

Time from ictus todeterioration (hr)

24

18

96

72

72

72

22

144

168

GCS, Glasgow Coma Scale; M, male; F, female; T, intubated(unable to evaluate verbal response of GCS); Dec, left hemiplegiaand right decerebrate posturing; An, right dilated pupil; FD, fixedand dilated right pupil.

cephalus were excluded as the etiology of neurologicdecline in these patients by emergency repeat headCT. When unilateral cerebral edema as a result ofright hemispheric infarction resulted in acute neuro-logic deterioration, patients were evaluated for righthemicraniectomy. When the clinical judgment of thephysicians was that medical therapy was ineffectiveand a fatal outcome was imminent, then emergencyright hemicraniectomy was performed. Surgicaldecompression of left hemispheric infarction was notperformed in this initial series of patients because ofconcern for the severe disability and poor quality oflife caused by aphasia and hemiplegia due to domi-nant hemisphere injury.

From August 1985 to April 1988, nine strokevictims (three men and six women with ages rangingfrom 41 to 68 years) with acute right cortical infarc-tions neurologically deteriorated while on medical

therapy (Table 1). One of these patients (case 1) haddeteriorated at his local hospital and was rapidlytransferred to the University of Virginia hospital fortreatment. In seven of these nine patients clinicalsigns of uncal herniation (anisocoria and/or rightdecerebrate posturing) accompanied neurologicdeterioration. Head CT demonstrated large rightmiddle cerebral distribution infarctions in all ninestroke victims. In addition, right anterior cerebraldistribution infarction was demonstrated in five ofthese patients. The range of time elapsed betweenonset of symptoms of acute cerebral infarction andfurther neurologic deterioration was 18-168 hourswith a median time of 72 hours. All nine patientswere thought to be poorly responsive to aggressivemedical modalities and were expected to expirewithout surgical decompression. Each of these ninestroke victims was treated for extensive unilateralcerebral edema by right hemicraniectomy.

The right cerebral hemisphere was surgicallydecompressed through a large hemicraniectomy (Fig-ure 1). The bone flap was removed and placed in coldstorage for future autologous cranioplasty. Addi-tional bone was removed in the temporal region tothe floor of the middle fossa. The dura was opened ina large cruciate incision involving the frontal, pari-etal, and temporal lobes. As the dura was opened,the pale infarcted brain typically began to herniateoutward. An intracerebral hematoma was resected inone patient (case 9) with hemorrhagic infarction.Cortical resection of infarcted brain was not per-formed in the other eight patients. In all ninepatients lyophilized cadaver dura was placed under-neath the incised dura and secured with severalsutures to allow the brain to herniate outward in amore controlled manner, as well as to prevent corti-

FIGURE 1. Schematic representation of right hemicraniectomy procedure. Left panel: After right hemicraniectomy, the dura isopened by a large cruciate incision to allow the brain to expand outward. The large bone flap is stored in cold storage for futurecranioplasty. Right panel: Lyophilized cadaver dura is then placed under the dura and secured with suture; the arrow indicates thisplacement.



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876 Stroke Vol 21, No 6, June 1990

TABLE 2. Patient Perioperative Glasgow Coma Scale Scores

Patient

1

2*

3

4

5

6

7

8

9

Before surgery

5T

11

12

3T

6T

4T

14

4T

6T

GCS

Day

7T

9T

12

9T

7T

8T

9T

9T

8T

After surgery

1 Day 7

14

10T

14

12

9T

14

15

14

6T

GCS, Glasgow Coma Scale; T, intubated (unable to evaluateverbal response of GCS).

*Died from lung cancer 1 month after surgery.

cal adhesions. The temporalis muscle and skin flapwere then reapproximated and secured with suture.

Patients were evaluated by the Glasgow ComaScale (GCS) and by neurologic examination beforeand after surgery (Tables 1 and 2). After dischargefrom the hospital, patients were also evaluated forfunctional independence by the Barthel Index (BI)scale (Table 3).1 This simple scale attempts to assessthe ability of a patient to care for himself. Thepatients and their significant others were asked aseries of questions to assess ability in self-care afterstroke and surgical decompression. A patient scoring100 by this scale is able to perform without assistancein activities of daily living, to walk at least a block,and to ascend and descend stairs. A score of 60-95indicates a patient who requires minimal assistancewith daily activities; a score of <60 implies that theindividual is functionally dependent. In addition tothe BI scale, patients and their significant otherswere asked the following question at home afterdischarge from the hospital: "Considering everythingthat has happened since the original surgery follow-ing the stroke (removal of the bone), if you had to

make the decision to have the surgery again, whatwould your answer be? Please rate your answer on ascale of 1 (yes) to 10 (no)."

ResultsPreoperative GCS scores and GCS scores 1 day

and 1 week after surgery are shown in Table 2. Sixpatients improved on the first postoperative dayfollowing right hemicraniectomy. Eight of the ninepatients demonstrated neurologic improvement onthe seventh postoperative day, and all nine patientssurvived the perioperative period. However, lungcancer was diagnosed in one patient (case 2) aftersurgical decompression had been performed; despitemarked neurologic improvement (GCS score of 14),she died 1 month later from a respiratory arrest whileundergoing pulmonary radiotherapy.

Patient outcome was evaluated in the eight surviv-ing patients by the BI score (Table 4). The BIevaluation was performed 5-25 months after righthemicraniectomy. Four patients (cases 1, 3, 5, and 8)were functioning at a level of assisted independence.The remaining four patients required assistance fromfamily members to accomplish typical tasks encoun-tered in their activities of daily living. All eightpatients were living at home with their families. Twopatients (cases 3 and 8) demonstrated a mild lefthemiparesis at the time of their BI evaluation; hemi-plegia was found in the other six stroke victims.Family members of each of the eight patients indi-cated that emotional lability had persisted sincecerebral infarction. Finally, subjective assessment ofthe surgical procedure and its outcome by the patientand a significant other was positive for all eightsurviving stroke victims (Table 4). Four of these eightpatients have returned for elective autologous bonecranioplasty.

During the same period, four other patients pre-sented with clinical signs of uncal herniation while onmedical therapy for large left hemispheric infarction.All four patients were hemiplegic on the right and

TABLE 3. Barthel Index

Index item

Score

Independent

10

5

5

10

10

10

10

15

15

10

With help

5

0

0

5

5

5

5

5-10

10

5

1. Feeding (food needs to be cut up=help)2. Bathing3. Personal toilet (wash face, comb hair, brush teeth, etc.)4. Dressing5. Bowel control (occasional accidents or needs enema or

suppository=help)6. Bladder control (occasional accidents or needs help with

collecting device=help)7. Toilet transfers8. Chair/bed transfers (minimal assistance=10; able to sit, but

needs maximum assistance to transfer=5)9. Ambulation (if unable to walk, but able to propel wheelchair)

10. Stair climbing (independent with assistive devices =• 10)



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FIGURE 2. Computed tomograms showing effects of largeright hemisphere stroke in 48-year-old man. Upper leftpanel: Early signs of infarction in the distribution of theright middle cerebral artery on admission. Upper rightpanel: Large right hemispheric infarct with mass effect andedema 3 days after ictus. Lower left panel: Right cranialdefect and decrease in shift of midline structures on firstday after hemicraniectomy.

densely aphasic. These patients did not undergosurgical decompression, and all four expired.

Of the nine patients who underwent hemicraniec-tomy, one (case 3) was a 48-year-old man who haddeveloped left lower extremity weakness the nightbefore admission. The following morning he hadawakened with a left hemiparesis. At the time ofadmission he was lethargic, but arousable and ori-ented. He had a blood pressure of 160/95 mm Hg,pulse of 70/min, and a right carotid bruit on auscul-

tation. Neurologic exam was remarkable for a GCS of14, right gaze preference with a left homonymoushemianopsia, and a severe left hemiparesis. Admis-sion head CT demonstrated early signs of infarctionin the distribution of the right middle cerebral artery(Figure 2, upper left). He was observed in theneurologic intensive care unit and treated with fre-quent intravenous mannitol bolus injections. Hebecame increasingly alert but had developed a lefthemiplegia with neglect. However, on the third day



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FIGURE 3. Computed tomogrums showing effects oflarge right cerebral infarction in 58-year-old woman.Upper left panel: Isodense area in right hemispheresuggesting infarction on admission. Upper right panel:Marked delineation of infarct with edema and shift ofmidline structures before surgery. Lower left panel:Large cranial defect with outward brain expansion andless cerebral shift toward the left 3 days after surgicaldecompression by hemicraniectomy.

after admission, he deteriorated with obtundation, aright dilated pupil, and a GCS of 12. After intuba-tion, the patient was hyperventilated, and an emer-gency head CT was performed. This demonstrated alarge right hemisphere infarct with mass effect andedema (Figure 2, upper right). Right hemicraniec-tomy with dural augmentation was then performed.Immediately after surgery, he was extubated andplaced on mannitol intravenous infusion of 5 mg/hr.His neurologic examination was unchanged on hisfirst postoperative day, but head CT demonstrated adecrease in shift of midline structures (Figure 2,

lower left). Over the ensuing days, he made markedimprovement; a GCS score of 14 was recorded on thefourth day after surgery. The patient was dischargedto home 17 days after hemicraniectomy, being alert,oriented, and hemiplegic on the left without neglect.When he was evaluated 9 months after surgicaldecompression, he lived at home, walked with a mildleft hemiparesis, and required minimal assistance inperforming his daily activities (BI score of 90).

Another of the hemicraniectomy patients (case 5)was a 58-year-old right-handed woman who pre-sented on admission with a history of developing



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Delashaw et al Hemicranlectomy for Cerebral Infarction 879

TABLE 4. Patient Barthel Index Score and Subjective AssessmentAfter Hemlcraniectomy

Patient1

3

4

5

6

7

8

9

Follow-up(mo)

14

9

22

15

15

5

25

17

BI score70

90

30

60

45

35

95

50

Subjective

Patient

:>

3

3

assessment*

Significantother

1

1

2

1

1

2

1

1

BI, Barthel Index. A BI score of 100 indicates a patient who isable to perform without assistance in activities of dairy Irving; ascore of 60-95 indicates a patient who requires minimal assistancewith dairy activities; a score of <60 implies that the patient isfunctionally dependent.

*For subjective assessment patients and their significant otherswere asked the following question at home after discharge fromthe hospital: "Considering everything that has happened since theoriginal surgery following stroke (removal of bone), if you had tomake the decision to have surgery again, what would your answerbe? Please rate your answer on a scale of 1 (yes) to 10 (no)."

acute left-sided weakness. Physical examination dem-onstrated a somnolent, but arousable and oriented,woman with a blood pressure of 130/84 mm Hg, pulseof 114/min, right gaze preference, left homonymoushemianopsia, and left hemiplegia (GCS of 14). A lowdensity area was seen on head CT in the distributionof the right middle cerebral artery suggesting a largehemispheric infarction (Figure 3, upper left). Shewas intubated, hyperventilated, and placed on amannitol intravenous infusion in the neurologicintensive care unit. Three days after admission, herneurologic examination showed her to be rapidlydeteriorating. She became markedly obtunded with afixed and dilated right pupil and a GCS score of 6T.Head CT demonstrated a large right hemisphericinfarction with edema and mass effect (Figure 3,upper right). A large right hemicraniectomy anddural augmentation were performed as emergencymeasures. Neurologic examination on the first dayafter surgery demonstrated anisocoria with reactivepupils and a GCS of 7T. Head CT performed 3 daysafter surgery demonstrated a large right hemisphericinfarct with less shift of midline structures (Figure 3,lower left). She was drowsy and remained intubatedfor 7 days after surgery but followed commands onexamination (GCS of 9T). She continued to improveneurologically and returned to the neurosurgicalservice for autologous cranioplasty 2 months aftersurgical decompression. She is currently living athome with her granddaughter. She is alert, oriented,and hemiplegic on the left, and she requires moder-ate assistance in performing everyday activities (BI of60 at 15 months after surgery).

DiscussionAlthough this is a small anecdotal series, hemi-

craniectomy with dural augmentation appears to be

an effective, lifesaving method of treating malignantcerebral edema secondary to stroke. The surgicaldecompressive procedure should be considered anadditional mode of therapy when contemporary med-ical therapy fails to curtail cerebral edema in strokevictims. All patients treated by hemicraniectomy sur-vived, but neurologic outcome was variable. Neuro-logic outcome following this procedure appears to becontingent on the location and extent of the infarc-tion and may also depend on the timing of thesurgery. Patients demonstrating neurologic declinewhile on medical therapy may benefit more fromhemicraniectomy if surgery is performed before clin-ical signs of uncal herniation.

Cerebral swelling following infarction results fromcytotoxic and vasogenic edema.2 Severe brain isch-emia initially produces cytotoxic edema withoutapparent disruption of the blood-brain barrier. Earlyischemia disturbs the regulatory mechanisms withincell membranes and results in the accumulation ofintracellular fluid. During this acute period, intravas-cular injections of protein-bound dyes fail to extrava-sate into the area of ischemia, and the infarct typi-cally is not visible on CT. However, as processes dueto the infarction progress, protein-bound fluids areable to diffuse across a damaged blood-brain barrierand to produce vasogenic cerebral edema.

Severe brain edema following cerebral infarction isa known cause of death in the acute infarctionperiod. Ng and Nimmannitya3 performed postmor-tem examinations of 353 consecutive cases of supra-tentorial cerebral infarction. Severe brain edema wasobserved in 45 of these patients. Acute brain edemaassociated with transtentorial herniation was attrib-uted as the cause of death in 35 of these 45 strokevictims. A high mortality rate has also been describedin stroke victims with large hemispheric infarctionswho present with neurologic deterioration. Ropperand Shafran4 described 12 patients who deterioratedduring their hospitalization for acute large cerebralinfarction. All 12 patients became drowsy, ninedeveloped asymmetric pupils or decerebrate postur-ing, and eight died. The cause of death in seven ofthe patients was attributed to cerebral edema; theother patient died as a result of systemic complica-tions. As demonstrated by our nine patients, craniec-tomy with dural augmentation can effectively reducemortality resulting from cerebral edema secondary tostroke.

Surgical decompression with removal of infarctedbrain has previously been shown effective in selectedcases with cerebellar infarction.5-7 Several casereports have also suggested that craniectomy may bean effective means of treating edema secondary tosupratentorial infarctions.8-12 Rengachary et al10

described three patients with acute right cerebralinfarction and uncal herniation who were treated byhemicraniectomy. All three of their patients survived.Two of these patients were left with severe neuro-logic deficits including hemiplegia; the other patient,15 years old, recovered with normal mentation and



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speech and a mild left hemiparesis. Young et al11 alsodescribed a case of a 59-year-old woman who dete-riorated 18 hours after presenting with a large righthemispheric infarction. An emergency right temporalcraniectomy and lobectomy was performed. Thepatient remained comatose for 48 hours and thenbegan to improve neurologically. After rehabilita-tion, she was alert, her speech was normal, and shecould walk with assistance. She remained with aspastic left hemiparesis. Ojemann et al9 have alsoreported that hemicraniectomy was effective in treat-ing two patients with large cerebral infarctions whodeveloped signs of brain stem compression.

Kondziolka and Fazl12 recently described the useof a more limited frontotemporal craniectomy in fivepatients with incipient cerebral herniation after cere-bral infarction. Their patients were significantlyyounger than our patients (mean age 40 years, range32-51 years). Their study included two patients withcerebral infarction in the setting of subarachnoidhemorrhage and aneurysm clipping, one patient withcarotid artery dissection, and one with presumedembolic infarction from an anterior communicatingartery aneurysm; the remaining patient had a moretypical presentation of a middle cerebral artery dis-tribution infarct. All of these patients were ambula-tory at the time of follow-up, with neurologic deficitsattributable to the original ischemic event.

Hemicraniectomy may be more effective for treat-ment of malignant edema related to stroke than fortreatment of head trauma. Cerebral stroke results ina unilateral mass of necrotic brain and edema with aviable contralateral hemisphere and brain stem.Decompressive craniectomy over the infarcted areamay prevent further ischemia and injury to theseviable areas. Edema that produces elevated intracra-nial pressure has also been treated in severe headtrauma by decompressive craniectomy; the resultshave varied.13"17 Severe head trauma is usually adiffuse process with irreversible bilateral cerebraland brain stem injury. Craniectomy for head traumamay not be as effective as in stroke because reductionof intracranial pressure and patient neurologic out-come may be limited in a diffusely damaged brain.Similarly, subarachnoid hemorrhage patients withischemia due to diffuse vasospasm may not respondas effectively to decompressive CTaniectomy as dopatients with spontaneous embolic or thromboticstroke.

In the management of patients with acute cerebralinfarction, physician objectives include the preserva-tion of life, prevention of extending cerebral injury,and avoidance of systemic complications. Patient age,family support, and potential neurologic outcomemust also be considered before aggressive manage-ment is undertaken. Hemicraniectomy for cerebralinfarction with severe edema may preserve life andprevent extension of central nervous system injury.Although surgical decompression of patients withsevere dominant hemisphere strokes may result insurvival, we would anticipate an extremely poor

quality of life. Patients who deteriorate while onmedical therapy for nondominant hemispheric infarc-tions are probably more suitable for hemicraniec-tomy. However, outcome in these patients can bevariable. Most patients will require extensive rehabil-itative therapy and lifelong assistance. A few patientsmay demonstrate dramatic improvement and pro-gress neurologically to a level where only minimalassistance is required. The variability in outcome isdependent on the location and extent of the infarc-tion, the patient's age, and possibly the timing ofsurgery. Young stroke victims, with a supportivefamily and a potential for neurologic recovery, areprobably more likely to have a favorable outcome.Therefore, when medical modalities fail to curtailcerebral edema in a young patient with nondominanthemispheric stroke, emergency hemicraniectomyshould be considered.

In conclusion, it was the opinion of the treatingphysicians that nine patients with massive right hemi-spheric infarction would die imminently from brainswelling unless the infarcted brain was decompressed.Hemicraniectomy was performed, and all patientsimproved, although one died 1 month later from anunrelated condition. The neurologic function in theother eight was variable, but the quality of life wasconsidered reasonable by the surviving patients andtheir families. Hemicraniectomy can be a lifesavingtreatment for massive right hemispheric infarction andcan provide a reasonable quality of life.

AcknowledgmentsThe authors are indebted to Mrs. Lucille Staiger

for editorial assistance and Mr. Craig Luce for illus-trative assistance.

References1. Mahoney FI, Barthel DW: Functional evaluation: The Barthel

index. Md Med J 1965;14:61-652. Katzman R, dasen R, Klatzo I, Meyer JS, Pappius HM, Waltz

AG: Brain edema in stroke: Study group on brain edema instroke. Stroke 1977;8:512-540

3. Ng LKY, Nimmannitya J: Massive cerebral infarction withsevere brain swelling: A clinicopathological study. Stroke 1970;1:158-163

4. Ropper AH, Shafran B: Brain edema after stroke: Ginicalsyndrome and intracranial pressure. Arch Neurol 1984;41:26-29

5. Duncan GW, Parker SW, Fisher CM: Acute cerebellar infarc-tion in the PICA territory. Arch Neurol 1975^32:364-368

6. Lehrich JR, Wintler GF, Ojemann RG: Cerebellar infarctionwith brainstem compression: Diagnosis and surgical treat-ment. Arch Neuwl 1970,22:496-498

7. Sypert GW, Alvord EC: Cerebellar infarction. Arch Neurol1975^2:357-363

8. Ivamoto HS, Numoto M, Donaghy RMP: Surgical decompres-sion for cerebral and cerebellar infarcts. Stroke 1974;5:365-370

9. Ojemann RG, Heros RC, Crowell RM: Surgical Managementof Cenbrovascular Disease. Baltimore, Md, Williams & WilkinsCo, 1988, p 143

10. Rengachary SS, Batnitsky S, Morantz RA, Arjunan K, JeffriesB: Hemicraniectomy for acute massive cerebral infarction.Neurosurgery 1981;321-328



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11. Young PH, Smith KR, Dunn RC: Surgical decompressionafter cerebral hemispheric stroke: Indications and patientselection. South Med J 1982;75:473-475

12. Kondziolka D, Fazl M: Functional recovery after decompres-sive craniectomy for cerebral infarction. Neurosurgery 1988;23:143-147

13. Britt RH, Hamilton RD: Large decompressive craniotomy intreatment of acute subdural hematoma. Neurosurgery 1978;2:195-200

14. Cooper PR, Rovit RL, Ransohoff J: Hemicraniectomy in thetreatment of acute subdural hematoma: A re-appraisal. SurgNeurol 1976;5:25-28

15. Kjellberg RN, Prieto A Jr: Bifrontal decompressive craniot-omy for massive cerebral edema. J Neurosurg 1971;34:488-493

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17. Venes JL, Collins WF: Bifrontal decompressive craniectomyin the management of head trauma. J Neurosurg 1975;49-433

KEY WORDS • brain edema • cerebral infarction • craniectomy



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Maggio and M S GradyJ B Delashaw, W C Broaddus, N F Kassell, E C Haley, G A Pendleton, D G Vollmer, W W

Treatment of right hemispheric cerebral infarction by hemicraniectomy.

Print ISSN: 0039-2499. Online ISSN: 1524-4628 Copyright © 1990 American Heart Association, Inc. All rights reserved.

is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231Stroke doi: 10.1161/01.STR.21.6.874

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